ArticleMolecular and cellular biology2003
The papillomavirus E8-E2C protein represses DNA replication from extrachromosomal origins.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- Inhibition of high risk HPV31 E8^E2 repressor activity enables differentiation-independent genome amplification and E4 expression.PLoS pathogens · 2026Article
- Article
- Comparative genomics and integrated system biology approach unveiled undirected phylogeny patterns, mutational hotspots, functional patterns, and molecule repurposing for monkeypox virus.Functional & integrative genomics · 2023Article
- Experimental Support for Human Papillomavirus Genome Amplification Early after Infectious Delivery.Journal of virology · 2023Article
- Human Papillomavirus Genome Copy Number Is Maintained by S-Phase Amplification, Genome Loss to the Cytosol during Mitosis, and Degradation in GJournal of virology · 2023Article
- A Critical Role for p53 during the HPV16 Life Cycle.Microbiology spectrum · 2022Article
- Review
- BRD4S interacts with viral E2 protein to limit human papillomavirus late transcription.Journal of virology · 2021Article
- EXPRESSION OF E8^E2 IS REQUIRED FOR WART FORMATION BY MOUSE PAPILLOMAVIRUS 1 IN VIVO.Journal of virology · 2021Article
- Epigenetic Regulation of the Human Papillomavirus Life Cycle.Pathogens (Basel, Switzerland) · 2020Review
- Inferring Virus-Host relationship between HPV and its host Homo sapiens using protein interaction network.Scientific reports · 2020Article
- Article
- Mucosal and Cutaneous Human Papillomavirus Infections and Cancer Biology.Frontiers in oncology · 2019Review
- A new cell culture model to genetically dissect the complete human papillomavirus life cycle.PLoS pathogens · 2018Article
- Identification and Functional Characterization of Phosphorylation Sites of the Human Papillomavirus 31 E8^E2 Protein.Journal of virology · 2018Article
- Interaction of NCOR/SMRT Repressor Complexes with Papillomavirus E8^E2C Proteins Inhibits Viral Replication.PLoS pathogens · 2016Article
- Initial amplification of the HPV18 genome proceeds via two distinct replication mechanisms.Scientific reports · 2015Article
- Characterization of the Human Papillomavirus 16 E8 Promoter.Journal of virology · 2015Article
- Recent Insights into the Control of Human Papillomavirus (HPV) Genome Stability, Loss, and Degradation.Journal of clinical medicine · 2015Article
- A novel recombinant papillomavirus genome enabling in vivo RNA interference reveals that YB-1, which interacts with the viral regulatory protein E2, is required for CRPV-induced tumor formation in vivo.American journal of cancer research · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Carcinogenic DNA viruses such as high-risk human papillomaviruses (HPV) and Epstein-Barr-Virus (EBV) replicate during persistent infections as low-copy-number plasmids. EBV DNA replication is restricted by host cell replication licensing mechanisms. In contrast, copy number control of HPV genomes is not under cellular control but involves the viral sequence-specific DNA-binding E2 activator and E8-E2C repressor proteins. Analysis of HPV31 mutant genomes revealed that residues outside of the DNA-binding/dimerization domain of E8-E2C limit viral DNA replication, indicating that binding site competition or heterodimerization among E2 and E8-E2C proteins does not contribute to copy number control. Domain swap experiments demonstrated that the amino-terminal 21 amino acids of E8-E2C represent a novel, transferable DNA replication repressor domain, whose activity requires conserved lysine and tryptophan residues. Furthermore, E8-E2C (1-21)-GAL4 fusion proteins inhibited the replication of the plasmid origin of replication of EBV, suggesting that E8-E2C functions as a general replication repressor of extrachromosomal origins. This finding could be important for the development of novel therapies against persistent DNA tumor virus infections.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.